Objective To explore the effect of Astragalus polysaccharides (APS) on the function and quantity of islet β cells in rats with type 2 diabetes mellitus (T2DM). Methods SD rats were randomly divided into normal control group, T2DM model group and APS treatment group, with 8 rats in each group. The T2DM rats in the T2DM model group was induced by the combination of high fat diet and streptozotocin, and the rats in the APS treatment group was treated with APS (700 mg·kg^-1·d^-1, content of APS being 70%). The rats were sacrificed after 8 weeks of drug intervention, and the serum samples were collected to measure fasting blood glucose (FBG), triglyceride (TG), total cholesterol (TC), high-density lipoprotein cholesterol (HDL-C), low-density lipoprotein cholesterol (LDL-C) and fasting insulin (FINS), and to calculate insulin secretion index (HOMA-β value). Pancreas tissues were extracted and stained with Hematoxylin-Eosin to observe the pancreatic histopathological characteristics, and the quantity of islet β cells was observed and calculated with immuno-histochemical method. Results (1) Compared with the normal control group, the rats in T2DM model group had significant increases in the FBG, TG and LDL-C, and significant decreases in the HDL-C, FINS and HOMA-β (P<0.05); compared with the T2DM model group, the rats in APS treatment group had significant decreases in the FBG, TG and LDL-C (P<0.05), and significant increases in the FINS and HOMA-β (P<0.05). (2) Compared with the normal control group, the rats in T2DM model group showed a significant atrophy of the islet accompanied by loss of granular and vacuolar degeneration, and the number of the islet β cells was significantly reduced (P<0.05); compared with the T2DM model group, the rats in APS treatment group showed a significant increase in the islet volume accompanied by improvement of islet degranulation and vacuolar degeneration, and had a significant increase in the number of islet β cells (P<0.05). Conclusion APS can improve the glucose and lipid metabolisms of the T2DM rats, which may be caused by increasing insulin secretion through the protective effect on pancreatic islet β cells.